Is the chemical prevention of gingivitis necessary to prevent severe periodontitis?
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Gingival inflammation seldom causes discomfort, social embarrassment or loss of function. As most sites with gingival inflammation do not progress to severe periodontal disease, gingivitis should not be considered a public health problem. Periodontitis is always preceded by gingivitis. But most gingivitis remains stable for years without progressing to periodontitis. The number of gingivitis sites that do convert is small. The levels of oral cleanliness achieved by the majority of populations in industrialized countries are below the threshold for severe destructive periodontal disease of personal and public health concern. Because methods of measuring the progression of periodontal disease are unreliable, definitive answers regarding conversion of gingivitis to severe periodontitis are lacking. Gingival inflammation frequently remains contained; most gingivitis remains stable for years without progressing to periodontitis. Decreasing gingivitis does reduce shallow pocketing, but the effect on severe periodontitis is not clear. Although the underlying justification for the reduction of plaque is to reduce gingival inflammation to prevent or reduce severe periodontitis and tooth loss, the basis for the approach is equivocal. A reasonably high level of plaque appears to be compatible with acceptably low levels of periodontal disease. Reducing nonspecific plaque levels to such levels is therefore a rational goal. The conventional methods of controlling periodontal disease involve mechanical removal of plaque and calculus. A complimentary ecological approach, using chemicals, would be to alter the environment of the pocket to prevent growth of putative pathogens. Any ecological approach should be sensitive to the dangers of disrupting the natural ecology of dental plaque. Some antimicrobial and antimetabolic agents such as fluoride, chlorhexidine and triclosan and zinc citrate can selectively suppress certain organisms or inhibit bacterial proteases implicated in tissue damage. The uncertainties about factors that convert gingival inflammation into periodontitis and periodontitis into severe periodontitis coupled with insufficient data from controlled clinical trials on the effectiveness of chemical reduction of gingivitis to prevent severe periodontitis leads one to conclude that more research is required before the need for the chemical prevention of gingivitis to prevent severe periodontitis can be justified.